FURTHER EVIDENCE FROM AN ELASTIC ARTERY THAT ANGIOTENSIN-II AMPLIFIES NORADRENALINE-INDUCED CONTRACTION THROUGH ACTIVATION OF PROTEIN-KINASE-C

Angiotensin II (AII, 0.1 nM) increased concentration dependently the sensitivity of rabbit aortic rings to low concentrations of noradrenaline. This was not associated with increases in noradrenaline-induced Ca-45(2+) uptake or efflux and was prevented by the protein kinase C (PKC) inhibitors staurosporine (0.01 muM) and calphostin C (0.1 muM). Pretreatment of the rings with PMA (phorbol-12-myristate-13-acetate, 0.1 and 1 muM, 24 h at 4-degrees-C) abolished the potentiation phenomenon. We conclude that AII potentiation of noradrenaline-induced vascular tone may be due to a PKC-mediated increase in intracellular sensitivity of the contractile apparatus to Ca2+.